Abstract Introduction Superior vena cava (SVC) syndrome results from the obstruction or occlusion of the SVC, leading to a range of complications depending on severity, location, and chronicity with the development of collateral circulation. We present a case of a patient with prior facial edema and subsequent development of bilateral pleural effusions whose evaluation led to discovery of SVC stenosis and occlusion of bilateral brachiocephalic veins, likely related to chronic indwelling pacemaker leads. Case Report A 73-year-old woman with bileaflet mitral valve prolapse with mild-to-moderate regurgitation, sinus node dysfunction status post pacemaker placement in 2014, atrial fibrillation and an unprovoked extensive right upper extremity deep venous thrombosis (DVT) managed on chronic apixaban therapy presented to clinic for evaluation of bilateral pleural effusions. One year prior to presentation, she developed facial and supraclavicular edema with positional dyspnea. A CT head and neck did not explain her abrupt facial edema though showed a left-sided pleural effusion, which was addressed locally with serial thoracenteses followed by tunneled pleural catheter placement. This ultimately led to discomfort without improvement in dyspnea, prompting catheter removal. She later developed a right-sided pleural effusion and underwent thoracentesis with the fluid analysis shown in Table 1. Physical exam was notable for collateral vessels along the chest wall and abdomen. The collateral vessels, unexplained pleural effusions, prior extensive right upper extremity DVT, and history of now resolved facial edema prompted CT venogram; this revealed occlusion of the right and left brachiocephalic veins and severe narrowing of the SVC with venous collaterals noted. PET-CT showed no evidence of malignancy. Electrophysiology consultation attributed the SVC stenosis to the indwelling pacemaker leads. The patient underwent SVC cavogram with successful angioplasty across right internal jugular vein down to the SVC with improvement in pressure gradient. After recanalization, there was no significant reaccumulation of pleural effusions on follow up and patient’s dyspnea improved. Discussion Pleural effusions in the setting of SVC syndrome have been described, most commonly due to thrombosis, device-related complications, or malignancy. This case highlights the importance of considering device-related vascular complications in patients with unexplained pleural effusions, particularly those with a history of intrathoracic devices or procedures. Management should target the underlying cause of the effusion; however long-term data on outcomes and optimal management strategies for pacemaker-related SVC syndrome remain limited. This abstract is funded by: None
Serafim et al. (Fri,) studied this question.